Haem Flashcards
Blood film post splenectomy
Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes
Fever, chills during blood transfusion
Non-haemolytic febrile reaction
Non-haemolytic febrile reaction management
Slow or stop the transfusion
Paracetamol
Monitor
Pruritus, urticaria during blood transfusion
Minor allergic reaction
Minor allergic reaction management
Temporarily stop the transfusion
Antihistamine
Non-haemolytic febrile reaction
Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage
Minor allergic reaction
Thought to be caused by foreign plasma proteins
Hypotension, dyspnoea, wheezing, angioedema during blood transfusion
Anaphylaxis
blood transfusion anaphylaxis management
Stop the transfusion
IM adrenaline
ABC support
oxygen
fluids
blood transfusion anaphylaxis management
Stop the transfusion
IM adrenaline
ABC support
oxygen
fluids
Fever, abdominal pain, hypotension during blood transfusion
Acute haemolytic reaction
Acute haemolytic reaction management
Stop transfusion
Confirm diagnosis
check the identity of patient/name on blood product
send blood for direct Coombs test, repeat typing and cross-matching
Supportive care
fluid resuscitation
Acute haemolytic reaction
ABO-incompatible blood e.g. secondary to human error
Pulmonary oedema, hypertension during blood transfusion
Transfusion-associated circulatory overload (TACO)
TACO management
Slow or stop transfusion
Consider intravenous loop diuretic (e.g. furosemide) and oxygen
TACO
Excessive rate of transfusion, pre-existing heart failure
Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension during blood transfusion
Transfusion-associated acute lung injury (TRALI)
TRALI management?
Stop the transfusion
Oxygen and supportive care
TRALI
Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood
Warfarin
reduction of vitamin K to its active hydroquinone form
* Prolong PT (extrinsic)
* Monitor using INR (as it involve PT and more efficient)
* 2,7,9,10
* War with your gf, she will become ur ex (extrinsic)
Unfractionated heparin
- 9,10,11,12
- High risk of osteoporosis and HIT
- Useful in renal failure and where high risk of bleeding (anticoagulation can be terminated rapidly)
- Protamine sulphate can reverse heparin effect completely
- Monitor APTT
LMWH (dalteparin, enoxaparin)
- 10
- Low risk of osteoporosis and HIT
- Not in renal failure
- Protamine sulphate reverse LMWH partially
- Monitor factor Xa (as the name RivaroXaban) however frequent monitoring not needed
- 1st line in VTE prophylaxis and treatment and ACS
Platelet transfusion for thrombocytopenia before surgery or an invasive procedure. Aim for plt levels of:
> 50×109/L for most patients
50-75×109/L if high risk of bleeding
100×109/L if surgery at critical site
Normoblastic causes of macrocytic anaemia
alcohol
liver disease
hypothyroidism
pregnancy
reticulocytosis
myelodysplasia
drugs: cytotoxics
Megaloblastic causes of macrocytic anaemia
Vit B12 deficiency
Folate deficiency (e.g. secondary to methotrexate)
Acute intermittent porphyria presentation
abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common
Acute intermittent porphyria
rare autosomal dominant condition caused by a defect an enzyme involved in the biosynthesis of haem
Tranexamic acid administration in major haemorrhage
IV bolus followed by slow infusion
effective if within 3 hours
What medication is contraindicated in T2DM and G6PD deficiency
sulphonyureas
Extrinsic pathway
Activation of TF (tissue factor) and factor VII
Intrinsic pathway
Factors VIII, IX, XI and XII activation
Common pathway
Factors V and X activation (converts prothrombin into thrombin)
Where thrombin then converts fibrinogen into fibrin
PT what pathway
extrinsic
APTT what pathway
intrinsic
Haemophilia A
Factor VIII deficiency
Haemophilia B
Factor IX deficiency
Vit K factors
II, VII, IX, X
APTT and PT in vw
normal PT, abnormal APTT, prolonged bleeding time
Haemophilia A and B inheritance
X-linked recessive
Von willebrand disease features
Excess or prolonged bleeding from minor wounds
Excess or prolonged bleeding post-operatively
Easy bruising
Menorrhagia
Epistaxis
GI bleeding
TTP pentad
Fever
Microangiopathic haemolytic anaemia (MAHA)
Thrombocytopaenic purpura
CNS involvement: headache, confusion, seizures
AKI
TTP treatment
Plasma exchange ASAP
Caplacizumab
Factor V leiden cause
mutation in clotting factor V, which becomes resistant to inactivation by protein C meaning it won’t turn off clotting
Protein C deficiency cause
Protein C (and its co-factor, protein S) inactivates clotting factors V and VIII. Inactivating mutations in protein C or S increase the risk of thrombosis
Antithrombin III function
inhibits factor IIa, Xa, IXa, and XI
Alpha thalassaemia presentation
Jaundice
Fatigue
Facial bone deformities
Alpha thalassaemia management
blood transfusions
stem cell transplant
splenectomy
Beta thalassaemia minor presentation
isolated microcytosis and mild anaemia
typically asymptomatic
Beta thalassaemia major presentation
Severe symptomatic anaemia at 3-9 months of age when levels of foetal haemoglobin fall
Frontal bossing
Maxillary overgrowth
Extramedullary hematopoiesis (hepatosplenomegaly).
Beta thalassaemia management
regular blood transfusions
consider iron chelating agent
